Evidence map›Paper›PMID 41465549›Full record

ReviewInternational journal of molecular sciences2025

Immunopathogenic Mechanisms in Connective Tissue Disease-Associated Interstitial Lung Disease: Incessant Loop of Immunity to Fibrosis.

Jae Ha Lee, Ji Hoon Jang, Sunggun Lee, Minyoung Her

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Jae Ha LeeDivision of Pulmonology and Critical Care Medicine, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan 48108, Republic of Korea.ORCID 0000-0003-0932-2826
Ji Hoon JangDivision of Pulmonology and Critical Care Medicine, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan 48108, Republic of Korea.
Sunggun LeeDivision of Rheumatology, Department of Internal Medicine, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan 48108, Republic of Korea.ORCID 0000-0003-3640-9185
Minyoung HerDivision of Rheumatology, Department of Internal Medicine, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan 48108, Republic of Korea.ORCID 0000-0002-2733-9501

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Connective tissue disease-associated interstitial lung disease (CTD-ILD) represents a significant cause of morbidity and mortality. It is characterized by the progressive convergence of chronic inflammation, immune dysregulation, and fibrotic remodeling in the lung parenchyma. While often conceptualized through a model of idiopathic pulmonary fibrosis (IPF), CTD-ILD is fundamentally an immune-driven pathology with distinct inflammatory mechanisms in which adaptive immunity plays a profound role. This narrative review explores the "inflammation-immunity-fibrosis continuum" in CTD-ILD, elaborating the intricate cellular and molecular pathways that distinguish it from IPF. We highlight the central role of persistent T-cell responses and B-cell dysregulation, which often occur within organized tertiary lymphoid structures in the lung. This review examines how these immune processes are propagated by multiple cytokine pathways, including the TGF-β/SMAD, JAK/STAT, and phosphodiesterase-4 signaling pathways, which serve as crucial links between inflammation and fibrosis. This distinct immune mechanism in CTD-ILD explains why immunomodulatory agents are a cornerstone of CTD-ILD treatment, in contrast to their limited efficacy in IPF, and emphasizes the current paradigm of combining immunosuppression with antifibrotic drugs to target the dual drivers of the disease.

Indexed as

Connective Tissue DiseasesLung Diseases, InterstitialAnimalsCytokinesFibrosisHumansIdiopathic Pulmonary FibrosisLungSignal TransductionCytokinesautoimmunityconnective tissue diseasesinterstitial lung diseasepulmonary fibrosisrheumatoid arthritissystemic sclerosis

Identifiers

PMID41465549
PMCPMC12732998

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.